title: Receptors for bradykinin and prostaglandin E2 coupled to Ca2+ signalling in rat cortical collecting duct.
abstract: In freshly isolated rat cortical collecting ducts (CCD) we measured intracellular Ca2+ activity ([Ca2+]j) with the Fura-2 method. Bradykinin (BK) induced a transient and biphasic increase in [Ca2+]j. This increase was concentration dependent and was half maximal at a concentration of 15 nM. The B2 receptor antagonist HOE 140 (100 nM, n = 6) completely abolished BK (100 nM) induced increase in [Ca2+]j. The B1 receptor agonist des-Arg9-bradykinin (100 nM, n = 4) had no effect on [Ca2+]j. In the absence of extracellular Ca2+, the maximal increase in [Ca2+]j, induced by BK was diminished and the secondary plateau phase was completely abolished. Prostaglandin E2 (PGE2) elevated [Ca2+]j, also concentration-dependently and biphasically. A half maximal effect was reached with 1 nM PGE2. The secondary plateau phase was absent when extracellular Ca2+ was removed. Sulprostone (100 nM, n = 6) mimicked the PGE2 (100 nM) induced increase in [Ca2+]j. The effect of BK (100 nM) on [Ca2+]j was not inhibited by the cyclooxygenase inhibitor indomethacin (10 microM, n = 5). Dopamine (1 microM, n = 4) did not significantly alter [Ca2+]j. BK and PGE2 regulate [Ca2+]j in the rat CCD via release of Ca2+ from intracellular Ca2+ stores as well as via Ca2+ influx from extracellular space. BK directly modulates [Ca2+]j, through B2 receptors. EP1 receptors are most likely to be responsible for the PGE2 induced increase in [Ca2+]j.
authors.affiliation: Medizinische Poliklinik, Westfälische Wilhelms-Universität, Münster, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Ankorina-Stark
authors.forename: S
authors.initials: S
authors.lastname: Haxelmans
authors.forename: E
authors.initials: E
authors.lastname: Schlatter
mesh_terms: D000818:Animals; D001920:Bradykinin / Q000378:metabolism / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D015232:Dinoprostone / Q000378:metabolism / Q000494:pharmacology; D004553:Electric Conductivity; D005260:Female; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018002:Receptors, Bradykinin / Q000819:agonists / Q000378:metabolism*; D018078:Receptors, Prostaglandin E / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D018002:Receptors, Bradykinin; D018078:Receptors, Prostaglandin E; D015232:Dinoprostone; D001920:Bradykinin; D002118:Calcium